Select your state to see jurisdictional framework, reporting obligations, and authority links. Substance information above is the same in every state.
Seizures Clinical criteria: The condition must be stable for the prescriber to consider the listed maximum quantity of this medicine suitable for this patient, AND Patient must have focal onset seizures; OR Patient must have primary generalised tonic-clonic seizures, AND The condition must have failed to be controlled satisfactorily by at least one other antiseizure medication. Treatment criteria: Must be treated by a health practitioner who is any of: (i) a medical practitioner, (ii) an authorised PBS prescriber who is not a medical practitioner, but who is: (a) sharing care of the patient with at least one medical practitioner; (b) intending to share care of the patient with a medical practitioner.
“The mechanism of action of oxcarbazepine and MHD is thought to be mainly based on blockade of voltage-sensitive sodium channels, thus resulting in stabilisation of hyperexcited neural membranes, inhibition of repetitive neuronal firing and diminishment of propagation of synaptic impulses.”
“Oxcarbazepine is rapidly eliminated from the plasma with apparent half-life values between 1.3 and 2.3 hours. In contrast, the apparent plasma half-life of MHD averaged 9.3 ± 1.8 h.”
Working under the parallel aged-care framework? Aged-care equivalent →
Curated subset. The full adverse-effect list is in the TGA Product Information; click any citation above to open it.
“The results demonstrate that oxcarbazepine and its pharmacologically active metabolite (the monohydroxy derivative, MHD) inhibit CYP2C19. In human liver microsomes, oxcarbazepine and MHD have little or no capacity to function as inhibitors for the following enzymes: CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, CYP4A9 and CYP4A11. Although inhibition of CYP 3A4/5 by oxcarbazepine and MHD did occur at high concentrations in vitro, it is not likely to be of clinical significance. Oxcarbazepine and MHD induce, in vitro and in vivo, the cytochromes CYP3A4 and CYP3A5 responsible for the metabolism of dihydropyridine calcium antagonists, oral contraceptives, and AEDs (e.g. carbamazepine), resulting in a lower plasma concentration of these drugs.”